tbuckley/cabot-search huggingface dataset:
Reply:
Authors: Kiran Bambha, Nathan M. Bass
Journal: Hepatology (2012)

We thank Dr. Holt for his interest in our study investigating associations between ethnicity and nonalcoholic fatty liver disease (NAFLD) using data from the Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN), and we appreciate the positive comments regarding our study made by Dr. Holt in his letter.1 Dr. Holt reiterates the importance of 2 key variables related to the analysis of NAFLD histologic severity, namely age and the role of the PNPLA3 rs738409 polymorphism that we had described in detail in the Discussion section of our article. We welcome Dr. Holt's reemphasis of our initial points. With respect to age, this is indeed a well-recognized risk factor associated with fibrosis in NASH. We specifically noted in our Discussion that "the lower frequency of advanced fibrosis may be explained, at least in part, by the overall younger age of the Latino population in [our] study."2-4 Additionally, as we stated in the original article, our investigation used a cross-sectional design, and therefore was not intended to address the fate of the patients at a more advanced age. Addressing this particular issue will require longitudinal follow-up and data collection, which may become feasible with ongoing and future follow-up of patients in the NASH CRN. With respect to the role of the PNPLA3 rs738409 polymorphism in the pathogenic differences between Latino and non-Latino white individuals, our Discussion emphasized the highly important potential role of this genetic variation and cited several pertinent studies from the rapidly growing literature on this topic.5-9 We appreciate Dr. Holt's citing the important study by Speliotes et al.10 Notably, this study was based, in part, on the same population in the NASH CRN that formed the basis for our investigation, and which further points to the emerging relationship between PNPLA3 and the pathogenesis of NASH. Additional studies are currently underway in the NASH CRN and in other collaborative groups that should shed more light on the complex genetic influences in NAFLD and other liver diseases. Kiran Bambha M.D., M.Sc.*, Nathan M. Bass M.D., Ph.D. , * Division of Gastroenterology and Hepatology, University of Colorado Denver, Aurora, CO, Department of Medicine, University of California San Francisco, San Francisco, CA.
Professional liability
Authors: M. J. Hatlie
Journal: JAMA (1989)

In 1987, a story in the<i>New York Times</i>(February 9, 1987;sect A:1) declared that the tort liability crisis of the mid-1980s was over. The reinsurance market was softening, claims frequency was stabilizing across the country, and tort reform had been achieved in Florida, the "Beirut of Medicine." One year later, a report issued by New York State's superintendent of insurance revealed that medical liability premiums in that state, frozen for years at artificially low rates, were endangering the solvency of its liability insurers and recommended immediate premium increases of up to 80%.<sup>1</sup>Florida's ceiling on noneconomic damages had been overturned in the courts, and insurers were nonrenewing more than 5000 physicians in the state while emergency department physicians were "on strike" (Associated Press, July 2, 1987). In the absence of a focused understanding of the many weaknesses of the tort compensation and quality assurance systems in its home
Hepatology Highlights
Authors: Zaid H. Tafesh, Robert S. Brown, Nicholas Russo, Russell Rosenblatt, Aleksey Novikov, Robert E. Schwartz, Joseph F. Pisa, Nicole T. Shen, Vikas Gupta, Shirley Cohen‐Mekelburg
Journal: Hepatology (2018)

Tafesh, Zaid H.; Brown, Robert S. Jr.; Russo, Nicholas; Rosenblatt, Russell; Novikov, Aleksey; Schwartz, Robert E.; Pisa, Joseph F.; Shen, Nicole T.; Gupta, Vikas; Cohen‐Mekelburg, Shirley Author Information
Erratum: Fyn tyrosine kinase, a downstream target of receptor tyrosine kinases, modulates antiglioma immune responses
Authors: Andrea Comba, Patrick J Dunn, Anna E Argento, Padma Kadiyala, Maria Ventosa, Priti Patel, Daniel B Zamler, Felipe J Nunez, Lili Zhao, Maria G Castro, Pedro R Lowenstein
Journal: Neuro-Oncology (2020)
Incorrect Y-Axis Labels and Minor Data Errors
Authors: David Brent, Giovanna Porta
Journal: JAMA (2019)

Karen C. Johnston, MD; Askiel Bruno, MD; Qi Pauls, MS; Christiana E. Hall, MD; Kevin M. Barrett, MD; William Barsan, MD; Amy Fansler, MPH; Katrina Van de Bruinhorst, MA; Scott Janis, PhD; Valerie L. Durkalski-Mauldin, PhD; for the Neurological Emergencies Treatment Trials Network and the SHINE Trial Investigators
FACTORS IN THE REGULATION OF RENAL ACTIVITY
Journal: JAMA (1923)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
A FEDERAL NARCOTIC DICTATOR
Journal: JAMA (1930)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Child-resistant containers a 'must' in drug-dispensing
Authors: P. Gunby
Journal: JAMA (1982)

Physicians who dispense pharmaceuticals must use child-resistant containers except when patients such as the elderly or handicapped would be unable to open them, according to the US Consumer Product Safety Commission. The commission monitors compliance with the federal Poison Prevention Packaging Act, and many states have parallel statutes. However, says David Schmeltzer, associate executive director of the commission's Directorate for Compliance and Administrative Litigation, the agency is concerned that some physicians who dispense pharmaceuticals themselves may not understand that they are subject to the law's packaging standards "in the same manner [as for] prescription drugs dispensed by pharmacists." The law provides that non-child-resistant packaging may be provided at a patient's request or a prescribing physician's direction, Schmeltzer concedes. But he emphasizes that this clearly "is to be the exception rather than the rule." Although children's accidental ingestions of aspirin and potentially poisonous substances of all kinds have declined by an
Immune system homeostasis during acute hepatitis C: Viral escape or T-cell regulation?
Authors: Fareed Rahman, Theo Heller, Barbara Rehermann
Journal: Hepatology (2004)

We are delighted that Perrella and colleagues agree with our interpretation of the observation that a sustained response to antiviral therapy was not associated with a lasting enhancement of HCV-specific T-cell responsiveness in the blood. As discussed in our publication,1 possible explanations include the compartmentalization of HCV-specific T cells in the liver, T-cell–independent mechanisms of interferon/ribavirin-induced HCV clearance, antiproliferative effects of interferon and lack of stimulation of HCV-specific T cells due to the rapid clearance of HCV antigens. At present, it is not possible to determine the relative contribution of each of these potential factors. A prospective analysis of spontaneously recovering patients with the same techniques and a systematic analysis of intrahepatic T-cell responses will be required to answer this intriguing question. As Perrella and colleagues have correctly stated, a direct effect of ribavirin on the cellular immune response was not discussed in our publication. This is because ribavirin has been described to stimulate Th1 responses2, 3 and we did not observe an increase of the HCV-specific Th1 response during interferon/ribavirin therapy. Finally, as we did not study any spontaneously recovered patients during the early, acute phase of hepatitis C, it was not possible to analyze the impact of regulatory T cells on the outcome of acute HCV infection. We do, however, agree with Perrella and colleagues that these are all important and interesting avenues of future research and are pleased that our study stimulates these questions. Fareed Rahman M.D.*, Theo Heller M.D.*, Barbara Rehermann M.D.*, * Liver Diseases Section, DDB, NIDDK, National Institutes of Health, DHHS, Bethesda, MD.
Molecular Biology
Journal: JAMA (2002)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Impairment of hemostasis in patients with severe hemophilia. Failure of diphenhydramine, chlorpromazine, and guaifenesin
Authors: G. R. Buchanan
Journal: JAMA (1978)

Twenty-three patients with severe hemophilia were given single or multiple doses of diphenhydramine hydrochloride, chlorpromazine hydrochloride, or guaifenesin to test their effects on hemostasis. In contrast with earlier studies with aspirin, bleeding times were not prolonged after ingestion of these three drugs. No patient had hemorrhage because of the drugs, and none recalled excessive bleeding following drug ingestion. These results greatly extend the clinical implications of prior observations carried out in normal subjects demonstrating that many antiplatelet drugs have no effects on in vivo hemostasis. We conclude that these drugs are probably safe for patients with bleeding disorders like hemophilia. (<i>JAMA</i>240:2173-2174, 1978)
Microarray-based gene expression profiles reliably predict ELISA-derived uPA and PAI-1 levels in breast cancer biopsies, a comparison between fresh frozen (FF) and formalin-fixed paraffin-embedded (FFPE) samples.
Authors: C. Matuschek, H. B. Prisack, E. Boelke, W. Budach, M. Peiper, M. Rezai, W. Janni, H. Bojar
Journal: Journal of Clinical Oncology (2011)

10555 Background: The urokinase plasminogen-activator (uPA) and its inhibitor (PAI-1) predict the benefit of node-negative breast cancer patients from chemotherapy. The determination of uPA and PAI-1 need(s) large amounts of tumor tissue. In contrast, microarray-based gene expression profiling (MGEP) requires only small quantities of FF tissue and is applicable to FFPE archival tissue. Identification of MPEG-derived surrogate markers for ELISA-based uPA/PAI-1 may facilitate their analysis together with MPEG-based predictive genes and metagenes. Methods: Three groups of breast cancer biopsies were analysed. Group A: 136 FF tissues from 2008-2009, Group B: 85 FF tissues from 2010, Group C: 20 independent FFPE tissues. Gene expression was assessed by Agilent 4x44K microarrays. Results: For group A a significant correlation between protein expression of uPA and uPA gene (PLAU) expression (r=0.627 p<0.001) and PAI-1 and PAI-1 genes (SERPINE1; r=0.281 p=0.001) was found. Top sets of genes correlated with uPA/PAI-1 protein expression were extracted. For group B additional sets of top correlated genes were identified. The correlation of individual genes with uPA/PAI-1 protein expression was highest for their genes themselves (PLAU: r=0.694 p<0.001; SERPINE1 (r=0.469 p<0.001). Subsequently consensus gene sets were identified with a good performance for both biopsy sets. Only genes which were significantly correlated with their counterparts in group C were selected, resulting in a final 11-gene model (uPA metagene) and a 6-gene model (PAI-1 metagene).They significantly correlated with uPA/PAI-1 protein expression in all groups of biopsies ( uPA: group A: r=0.621, p<0.001; group B: r=0.771, p<0.001; group C: r=0.665, p=0.005; for PAI-1: group A: r=0.569, p<0.001; group B: r=0.687, p<0.001; Group C: r=0.683, p=0.008). Conclusions: Reliable MPEG-derived metagenes as surrogate markers for ELISA-based uPA/PAI-1 expression were identified.
Errors in Red and White Blood Cell Counts
Authors: Chujun Wu, Dongsheng Fan
Journal: JAMA Neurology (2018)

Michael R. Wilson, MD, MAS; Brian D. O’Donovan, MS; Jeffrey M. Gelfand, MD, MAS; Hannah A. Sample, BS; Felicia C. Chow, MD, MAS; John P. Betjemann, MD; Maulik P. Shah, MD; Megan B. Richie, MD; Mark P. Gorman, MD; Rula A. Hajj-Ali, MD; Leonard H. Calabrese, DO; Kelsey C. Zorn, MHS; Eric D. Chow, PhD; John E. Greenlee, MD; Jonathan H. Blum, MD, PhD; Gary Green, MD; Lillian M. Khan, BS; Debarko Banerji, BS; Charles Langelier, MD, PhD; Chloe Bryson-Cahn, MD; Whitney Harrington, MD, PhD; Jairam R. Lingappa, MD, PhD; Niraj M. Shanbhag, MD, PhD; Ari J. Green, MD, MAS; Bruce J. Brew, MBBS, DMedSci, DSc; Ariane Soldatos, MD; Luke Strnad, MD; Sarah B. Doernberg, MD, MAS; Cheryl A. Jay, MD; Vanja Douglas, MD; S. Andrew Josephson, MD; Joseph L. DeRisi, PhD
Disciplining doctors.
Journal: BMJ (1987)

Self injury and mental handicap SIR,-Like suicide, self injury is a form of self mutilation and is not always a form of attention seeking due to boredom, as Dr Brian Kirman assumes (31 October, p 1086).Suicide and self mutilation are often forms of aggression turned inwards and associated with aggression to others.This is particularly true ofthe mentally retarded.Control ofaggression is difficult but notoriously so in those severely retarded.'From 1969 onwards there have been several reports on the usefulness of lithium in patients exhibiting aggression.The patients included groups of delinquents, psychotics, and the ment- ally handicapped.The larger studies indicate a positive response in some 70-75% of cases.2These figures were confirmed in the first published multicentre double blind trial of lithium in mentally handicapped patients, published last May.3Until the survey quoted by Dr Kirma. is published it is not possible to say whether the authors were aware of this but it seems unlikely.Lithium is not necessarily a cure and is usually given only when all other methods have failed, although a plea for its earlier use in these patients was made recently.5It seems helpful in relieving aggression, including self mutilation, in these patients, which distresses them, their relatives, and staff.The grave shortages of staff trained in behavioural techniques may to some extent be relieved if this element is used with effect.The patient may become more receptive to this type of treatment.
Is medical diagnosis a general computer problem?
Authors: T. D. Sterling
Journal: JAMA (1966)

An excellent and concise summary of the rationale for the intermittent concern some physicians have shown about the possible assistance computers may render the diagnostician was recently advanced by Bruce and Yarnall.<sup>1</sup>Whenever he makes a decision on diagnosis, prognosis, or choice of therapy, the physician faces the possibility of being "wrong." Can the computer help minimize the number and seriousness of such errors? Allegations and claims concerning the ability of computers to function as diagnosticians have accompanied the growth of medical computer applications from the beginning. Sufficient experience with computers has accumulated by now so that we can examine the possibility of computer-based diagnosis more critically. Such a careful evaluation is also called for because many astute and thoughtful physicians have been repelled by exaggerated and misinformed claims of what the computer can and cannot do. These exaggerations detract from the real service computers can eventually and indeed
Nouveau traité de médecine.
Journal: JAMA (1930)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
PWE-174 Eosinophilic oesophagitis: biopsy protocol and histological reporting fall short of recommendations
Authors: B White, E Dhesi, A Joshi, K Besherdas
Journal: Gut (2015)

<h3>Introduction</h3> Eosinophilic Oesophagitis (EoE) is an increasing clinical problem. Patients with EoE commonly present with dysphagia, food impaction, chest pain unresponsive to antacids, and gastro-oesophageal reflux disease (GORD) like symptoms. To confirm a diagnosis of EoE, it is highly recommended to obtain oesophageal biopsies following trial of high-dose proton pump inhibitor therapy (to exclude GORD which may also have microscopic eosinophilia). Sampling from both normal and abnormal appearing areas with a minimum of 4 biopsies (each proximal and distal oesophagus) is recommended. Doing 6–9 biopsies increases the sensitivity of detecting EoE to 100%. Histologically, the diagnosis of EoE is made in presence of at least 15 eosinophils per high-power field (hpf) and should be documented in the microscopic histopathology report. <h3>Method</h3> A single centre, retrospective analysis, of patients with a diagnosis of EoE at a large NHS Hospital Trust in north London over 4 years from 2010 was performed. The database of patients was obtained from histology department. The endoscopy and histology report of the patients were analysed for the number of biopsies obtained (protocol recommends 8), site at which biopsies were obtained (protocol recommends proximal and distal oesophagus) and presence of &gt; 15 eosinophils per hpf within the histology report. <h3>Results</h3> During the study period, 29 patients with EoE were identified. The number of biopsies obtained varied from 1–8 (mean 3.5). One patient had 8 biopsies. 28/29 patients had 7 or less biopsies obtained. No patient had at least 4 biopsies from 2 different sites, with 15 (52%) having biopsy from lower oesophagus, 10 (30%) from mid oesophagus, 2 (7%) from middle and upper oesophagus and 1 (3%) from upper and lower oesophagus, One had biopsies fromupper, middle and lower oesophagus. In 6 of 29 (20%),the histopathology report explicitly mentioned the presence of &gt;15 eosinophils per hpf. <h3>Conclusion</h3> From this study, we conclude that biopsy protocol for diagnosis of EoE falls short of the consensus recommendations, not only in the total number of oesophageal biopsies obtained but also location from which biopsies are obtained. In only 83% of patients was the recommended diagnostic criteria of &gt;15 eosinophils per hpf used. If biopsy and reporting protocol is not followed there is a risk that patients with another cause of raised eosinophils (eg GORD) may be incorrectly diagnosed with EoE. We recommend a greater awareness and observation of the protocol for obtaining biopsies and its histology reporting in EoE. <h3>Disclosure of interest</h3> None Declared.
Salmonella
Authors: A Hoekstra
Journal: JAMA (2007)

tomatoes should be refrigerated within 2 hours or discarded.Refrigeration of cut tomatoes at 40°F (4.4°C) is needed to maintain both quality and safety.Cut tomatoes should be separated from raw, unwashed produce items, raw meats, and raw seafood.To prevent future tomato-associated outbreaks of Salmonella infections, further environmental and laboratory researchisnecessarytodeterminethesource androutesofcontamination,mechanisms bywhichpathogenscontacttomatoesand become internalized, the stages of development at which plants are most susceptible to contamination that persists, and procedures by which contamination can bereducedoreliminated.Towardthisend, the North American Tomato Trade Work GrouppublishedCommoditySpecificFood SafetyGuidelinesfortheFreshTomatoSupply Chain in May 2006 to promote adoption of good agricultural practices throughoutthefreshtomatosupplychain.Traceback investigations in future outbreaksshouldconsideralllevelsoftomato production, including the field and packinghouse.Studies focused on these areas should be a priority for the agricultural industry, food safety agencies, and the public health community.